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Cytokine expression in malaria-infected non-human primate placentas

机译:细胞因子在疟疾感染的非人类灵长类胎盘中的表达

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摘要

Malaria parasites are known to mediate the induction of inflammatory immune responses at the maternal-foetal interface during placental malaria (PM) leading to adverse consequences like pre-term deliveries and abortions. Immunological events that take place within the malaria-infected placental micro-environment leading to retarded foetal growth and disruption of pregnancies are among the critical parameters that are still in need of further elucidation. The establishment of more animal models for studying placental malaria can provide novel ways of circumventing problems experienced during placental malaria research in humans such as inaccurate estimation of gestational ages. Using the newly established olive baboon (Papio anubis)-Plasmodium knowlesi (P. knowlesi) H strain model of placental malaria, experiments were carried out to determine placental cytokine profiles underlying the immunopathogenesis of placental malaria. Four pregnant olive baboons were infected with blood stage P. knowlesi H strain parasites on the one fiftieth day of gestation while four other uninfected pregnant olive baboons were maintained as uninfected controls. After nine days of infection, placentas were extracted from all the eight baboons through cesarean surgery and used for the processing of placental plasma and sera samples for cytokine sandwich enzyme linked immunosorbent assays (ELISA). Results indicated that the occurrence of placental malaria was associated with elevated concentrations of tumour necrosis factor alpha (TNF-α) and interleukin 12 (IL-12). Increased levels of IL-4, IL-6 and IL-10 and interferon gamma (IFN-γ) levels were detected in uninfected placentas. These findings match previous reports regarding immunity during PM thereby demonstrating the reliability of the olive baboon-P. knowlesi model for use in further studies.
机译:已知疟原虫会在胎盘疟疾(PM)期间介导母体-胎儿界面的炎症性免疫反应,从而导致不良后果,如早产和流产。导致疟疾感染的胎盘微环境中发生的导致胎儿发育迟缓和怀孕中断的免疫学事件仍然是需要进一步阐明的关键参数。建立更多的用于研究胎盘疟疾的动物模型可以提供新颖的方法来解决人类胎盘疟疾研究中遇到的问题,例如对胎龄的不正确估计。使用新建立的橄榄狒狒(Papio anubis)-诺氏疟原虫(P. Knowlesi)H胎盘疟疾模型,进行实验以确定胎盘疟疾免疫发病机制的胎盘细胞因子谱。在妊娠的第五十天,有四个怀孕的橄榄狒狒被感染了血液阶段的诺氏杆菌H菌株寄生虫,而其他四个未感染的怀孕橄榄狒狒则被作为未感染的对照。感染9天后,通过剖宫产术从所有8只狒狒中提取胎盘,并用于处理胎盘血浆和血清样品,进行细胞因子夹心酶联免疫吸附测定(ELISA)。结果表明,胎盘疟疾的发生与肿瘤坏死因子α(TNF-α)和白介素12(IL-12)浓度升高有关。在未感染的胎盘中检测到IL-4,IL-6和IL-10和干扰素γ(IFN-γ)水平升高。这些发现与先前关于PM期间免疫力的报道相符,从而证明了橄榄狒狒-P的可靠性。 Knowlesi模型可用于进一步研究。

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